Computational modeling
Finite element modeling
Finite element models can provide predictions of stress and strain distributions in complex, fiber-reinforced tissues, which may be difficult or impossible to measure experimentally. Additionally, the models can also be used to guide experimental designs for studies that are time- or cost-intensive.
Our group has developed both tissue- and joint-level finite element models. The multiscale, structure-based tissue-level model is rigorously validated under multiple loading modalities, loading conditions, and boundary conditions, allowing us to simultaneously investigate both tissue- and subtissue-level mechanics. The model also has the potential to directly evaluate fiber-matrix interactions. The joint-level model is validated under multiple loading modalities and enables us to assess the effect of degeneration and combined multiaxial loading on disc mechanics.
Tissue-level multiscale, structure-based finite element models
Representative model-predicted annulus fibrosus tissue-level stress and strain distributions under uniaxial tension
Joint-level FEMs for bovine lumbar discs
If you are interested in the most recent finite element modeling research updates, please feel free to contact Minhao Zhou (minhao dot zhou at berkeley dot edu).
Molecular dynamics simulation
Changes occurring at the cellular scale are linked to changes at the molecular scale, and vice versa. For example, in tissue engineering, cartilage cells (chondrocytes) lose their phenotype, or dedifferentiate, during 2D expansion – indicated by changes in gene expression and cell shape. During expansion, the cell’s outside environment and the distribution of the forces on the cell are altered. A force-sensitive biomolecule at the boundary of the cell is the adhesion molecule, integrin, which is a key player in transmitting these forces from outside the cell to inside the cell. We aim to understand how multiscale mechanical effects at the cell boundary lead to changes in cell shape, indicative of chondrocyte dedifferentiation, by coupling a single-cell finite element (FE) model with a cell adhesion molecular dynamics (MD) model. By gaining this mechanistic insight, we can then optimize tissue engineering and cartilage repair strategies at both the molecular and cell scales.
If you are interested in the most recent coupled molecular dynamics and finite element modeling updates, please feel free to contact Andre Montes (amontes at berkeley dot edu).